The overall aim of the present investigation is to elucidate the functions of the eosinophil in allergic reactions. Eosinophils are predominant at sites where allergic inflammatory reactions occur, however, the role played by these cells is unclear. Evidence obtained from in vitro studies indicate that eosinophils are attracted to reacting sites by at least two chemical mediators; the eosinophil chemotactic factor of anaphylaxis (ECF-A) and histamine. Further evidence suggests that the accumulated eosinophils may limit or dampen the extent of allergic inflammation. This latter is thought to be accomplished by the release of a number of recently described eosinophil constituents, i.e., arylsulfatase, histaminase, a major basic protein (MBP), phospholipase D and an eosinophil-derived-inhibitor (EDI). While such a modulatory function for the eosinophils is an attractive one, no corroborative in vivo data are available. The present proposal is designed to gain such in vivo evidence. Localized cutaneous eosinophilia followed by localized allergic reactions are to be induced in allergic humans and sensitized guinea pigs. The extent of eosinophilic infiltration, release of eosinophil derived products, the influence of eosinophils and/or their constituents on the development of the allergic reaction as well as the nature and extent of mediator(s) released will be all assessed by analyzing the cellular and humoral contents of skin chambers applied over such reacting sites. Local eosinophilia will be induced with histamine or ECF-A. Released histamine will be assayed fluorimetrically, PAF by platelet aggregation and EDI through its ability to inhibit leukocyte histamine release and affect platelet aggregation. The PGE content of EDI will be measured by RIA and its prostaglandin nature ascertained by mass spectrometry. Histaminase is to be assessed by radiochromatograms, and further corroborative evidence for the presence of IgE on eosinophils established by immunoferritin techniques and electron mciroscopy.